ArticleScientific reports2015
Effect of N-n-butyl haloperidol iodide on ROS/JNK/Egr-1 signaling in H9c2 cells after hypoxia/reoxygenation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Liproxstatin-1 Attenuates Retinal Ischemia-Reperfusion Injury by Suppressing EGR1-Mediated Ferroptosis.Antioxidants (Basel, Switzerland) · 2026Article
- In vivo toxic and lethal cardiorespiratory effects of a synthetic quaternary ammonium salt derivative of haloperidol in mice.Animal models and experimental medicine · 2025Article
- Early Growth Response 1 Contributes to Renal IR Injury by Inducing Proximal Tubular Cell Apoptosis.International journal of molecular sciences · 2023Article
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- JNK-dependent phosphorylation and nuclear translocation of EGR-1 promotes cardiomyocyte apoptosis.Apoptosis : an international journal on programmed cell death · 2022Article
- N-n-Butyl haloperidol iodide ameliorates liver fibrosis and hepatic stellate cell activation in mice.Acta pharmacologica Sinica · 2022Article
- Glycyrrhizic acid exerts protective effects against hypoxia/reoxygenation-induced human coronary artery endothelial cell damage by regulating mitochondria.Experimental and therapeutic medicine · 2020Article
- Versatile Nanoplatforms with enhanced Photodynamic Therapy: Designs and Applications.Theranostics · 2020Review
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- Ripk3 promotes ER stress-induced necroptosis in cardiac IR injury: A mechanism involving calcium overload/XO/ROS/mPTP pathway.Redox biology · 2018Article
- Egr-1 mediates leptin-induced PPARγ reduction and proliferation of pulmonary artery smooth muscle cells.Molecular biology of the cell · 2018Article
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- Self-nanomicellizing solid dispersion of edaravone: part I - oral bioavailability improvement.Drug design, development and therapy · 2018Article
- Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation.Experimental and therapeutic medicine · 2017Article
- NLRP3 Inflammasome Activation-Mediated Pyroptosis Aggravates Myocardial Ischemia/Reperfusion Injury in Diabetic Rats.Oxidative medicine and cellular longevity · 2017Article
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- Age-associated up-regulation of EGR1 promotes granulosa cell apoptosis during follicle atresia in mice through the NF-κB pathway.Cell cycle (Georgetown, Tex.) · 2016Article
- Article
- The c-Jun N-terminal kinase (JNK) pathway is activated in human interstitial cystitis (IC) and rat protamine sulfate induced cystitis.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS)-induced oxidative stress in cells is an important pathophysiological process during myocardial ischemia/reperfusion (I/R) injury, and the transcription factor Egr-1 is a master switch for various damage pathways during reperfusion injury. An in vitro model of myocardial I/R injury and H9c2 cardiomyoblast cells hypoxia/reoxygenation (H/R) was used to assess whether there is abnormal intracellular ROS/JNK/Egr-1 signaling. We also assessed whether N-n-butyl haloperidol (F2), which exerts protective effects during myocardial I/R injury, can modulate this pathway. H/R induced ROS generation, JNK activation, and increased the expression of Egr-1 protein in H9c2 cells. The ROS scavengers edaravone (EDA) and N-acetyl-L-cysteine (NAC) reduced ROS level, downregulated JNK activation, and Egr-1 expression in H9c2 cells after H/R. The JNK inhibitor SP600125 inhibited Egr-1 overexpression in H9c2 cells caused by H/R. F2 could downregulate H/R-induced ROS level, JNK activation, and Egr-1 expression in H9c2 cells in a dose-dependent manner. The ROS donor hypoxanthine-xanthine oxidase (XO/HX) and the JNK activator ANISO antagonized the effects of F2. Therefore, H/R activates ROS/Egr-1 signaling pathway in H9c2 cells, and JNK activation plays an important role in this pathway. F2 regulates H/R-induced ROS/JNK/Egr-1 signaling, which might be an important mechanism by which it antagonizes myocardial I/R injury.
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